Miehlke S, Kibler K, Kim J G, Figura N, Small S M, Graham D Y, Go M F
Veterans Affairs Medical Center, Houston, Texas 77030, USA.
Am J Gastroenterol. 1996 Jul;91(7):1322-5.
Helicobacter pylori is an important factor in the development of duodenal ulcer disease and has been implicated in the pathogenesis of gastric adenocarcinoma. It has been suggested that the cagA gene is a marker for more virulent strains of H. pylori.
We determined the prevalence of the cagA gene in 60 clinical isolates [34 from gastric carcinoma patients (CA), 26 from duodenal ulcer patients (DU)] from Korea, a country with a high incidence and mortality from gastric cancer. Genomic DNA was polymerase chain reaction-amplified by using two different primer sets for the cagA gene. The first cagA primer set amplifies a 297-bp product from the midregion of the cagA gene. The second primer set, which was previously established in a patient population from the Houston area (21 DU patients, 20 from individuals with asymptomatic gastritis) amplified a 1.4-kb region further downstream in the cagA gene.
The expected 297 bp polymerase chain reaction amplicon for cagA was identified in 59/60 (98.3%) H. pylori isolates from Korea (33/34 CA, 26/26 DU), and in 36/41 (88%) isolates from the Houston area (20/21 DU, 16/20 asymptomatic gastritis) (NS). Using the second cagA primer set, the expected 1.4-kb product was found in only 1/60 (1.7%) H. pylori isolates from Korea (1/34 CA, 0/26 DU), and in 36/41 (88%) of isolates from the Houston area (20/21 DU, 16/20 GST) (p < 0.001). Western blot analysis showed that all Korean H. pylori isolates expressed cagA.
The high prevalence of the cagA gene in H. pylori isolates from Korean patients with gastric adenocarcinoma or duodenal ulcers indicates that the cagA gene is common in H. pylori strains, and therefore, is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. Our data further suggest that allelic variations in the genome of H. pylori strains may exist and that distinct H. pylori populations may circulate in different geographic regions.
幽门螺杆菌是十二指肠溃疡疾病发展的一个重要因素，并且与胃腺癌的发病机制有关。有人提出，cagA基因是幽门螺杆菌更具毒性菌株的一个标志物。
我们测定了来自韩国的60株临床分离株（34株来自胃癌患者（CA），26株来自十二指肠溃疡患者（DU））中cagA基因的流行情况，韩国是一个胃癌发病率和死亡率都很高的国家。使用两种不同的cagA基因引物对基因组DNA进行聚合酶链反应扩增。第一对cagA引物扩增出cagA基因中部区域的一个297 bp产物。第二对引物是先前在休斯顿地区的患者群体（21例DU患者，20例无症状胃炎个体）中建立的，它扩增出cagA基因下游更远位置的一个1.4 kb区域。
在来自韩国的59/60（98.3%）株幽门螺杆菌分离株（33/34 CA，26/26 DU）中鉴定出了预期的297 bp cagA聚合酶链反应扩增子，在来自休斯顿地区的36/41（88%）株分离株（20/21 DU，16/20无症状胃炎）中也鉴定出了该扩增子（无显著差异）。使用第二对cagA引物，仅在来自韩国的1/60（1.7%）株幽门螺杆菌分离株（1/34 CA，0/26 DU）中发现了预期的1.4 kb产物，而在来自休斯顿地区的36/41（88%）株分离株（20/21 DU，16/20 GST）中发现了该产物（p<0.001）。蛋白质免疫印迹分析表明，所有韩国幽门螺杆菌分离株都表达cagA。
在韩国胃癌或十二指肠溃疡患者的幽门螺杆菌分离株中cagA基因的高流行率表明，cagA基因在幽门螺杆菌菌株中很常见，因此，作为区分幽门螺杆菌菌株与特定疾病关系的单一标志物并不可靠。我们的数据进一步表明，幽门螺杆菌菌株基因组中可能存在等位基因变异，并且不同的幽门螺杆菌群体可能在不同地理区域传播。
